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Evidence Based Pediatrics and Child Health is a ground-breaking new text on pediatrics and child care management, using evidence based approach. It covers all the major childhood conditions and contains the features of both a handbook and a reference text. Each chapter combines both advice on management and how best to practice evidence based medicine with reviews of all the available evidence in a specific area. The goal of the book is to help pediatricians and others who care for children to provide the best possible care by combining the best, most current evidence with special circumstances of each individual patient.
Intermittent hypoxia can cause significant structural and functional impact on the systemic, organic, cellular and molecular processes of human physiology and pathophysiology. This book focuses on the most updated scientific understanding of the adaptive (beneficial) and maladaptive (detrimental) responses to intermittent hypoxia and their potential pathogenetic or prophylactic roles in the development and progression of major human diseases. This is a comprehensive monograph for clinicians, research scientists, academic faculty, postgraduate and medical students, and allied health professionals who are interested in enhancing their up-to-date knowledge of intermittent hypoxia research and its translational applications in preventing and treating major human diseases.
Bringing together top-level contributions on all aspects of the subject, this book provides an overview of the recent advances in the genetics of respiratory control in health and disease. It also shows how combined studies in humans and mouse models have helped to improve our understanding of the mechanisms that underlie genetically determined respiratory control disorders with the goal of developing new therapeutic interventions.
Brain Hypoxia and Ischemia explores the various aspects of cell death and survival that are crucial for understanding the basic mechanisms underlying brain hypoxia and ischemia. Chapters focus on a panorama of issues including the role of ion channels/transporters, mitochondria and apoptotic mechanisms, the roles of glutamate/NMDA, mechanisms in penumbral cells and the importance of intermittent hypoxia and gene regulation under these stressful conditions. The volume explores findings from both mammalian and invertebrate model systems and their applicability to human systems and diseases. Careful consideration is also given to differences in hypoxia and ischemia across development. This volume aims to increase the understanding of these mechanisms and to stimulate research on better diagnosis and treatment of diseases that afflict the brain and potentially other organs when O2 levels are dysregulated. Brain Hypoxia and Ischemia is designed for neuroscientists, clinicians and medical/graduate students for use in both basic research and clinical practice.
The molecular deprivation of oxygen is manifested by hypoxia, a deficiency of oxygen and anoxia, or the absence of oxygen supply to the tissues. This book entitled Hypoxia and Anoxia will cover a broad range of understanding on hypoxia and anoxia from molecular mechanisms to pathophysiology. Hypoxia and anoxia stimulate multiple systems through specific cell signal transduction pathways and regulate several transcriptional factors like HIF-1, REST to encode genes for VEGF, Epo, etc. This book will also highlight different types of hypoxia and anoxia along with their impact on apoptosis, cardiovascular pathophysiology, and glucose regulatory mechanisms. This book will be a ready reckoner to give a deep understanding of the oxygen-sensing environment in vivo for researchers, academicians, and clinicians throughout the world.
In the past, ‘traditional’ moderate-intensity continuous training (60-75% peak heart rate) was the type of physical activity most frequently recommended for both athletes and clinical populations (cf. American College of Sports Medicine guidelines). However, growing evidence indicates that high-intensity interval training (80-100% peak heart rate) could actually be associated with larger cardiorespiratory fitness and metabolic function benefits and, thereby, physical performance gains for athletes. Similarly, recent data in obese and hypertensive individuals indicate that various mechanisms – further improvement in endothelial function, reductions in sympathetic neural activity, or in arterial stiffness – might be involved in the larger cardiovascular protective effects associated with training at high exercise intensities. Concerning hypoxic training, similar trends have been observed from ‘traditional’ prolonged altitude sojourns (‘Live High Train High’ or ‘Live High Train Low’), which result in increased hemoglobin mass and blood carrying capacity. Recent innovative ‘Live Low Train High’ methods (‘Resistance Training in Hypoxia’ or ‘Repeated Sprint Training in Hypoxia’) have resulted in peripheral adaptations, such as hypertrophy or delay in muscle fatigue. Other interventions inducing peripheral hypoxia, such as vascular occlusion during endurance/resistance training or remote ischemic preconditioning (i.e. succession of ischemia/reperfusion episodes), have been proposed as methods for improving subsequent exercise performance or altitude tolerance (e.g. reduced severity of acute-mountain sickness symptoms). Postulated mechanisms behind these metabolic, neuro-humoral, hemodynamics, and systemic adaptations include stimulation of nitric oxide synthase, increase in anti-oxidant enzymes, and down-regulation of pro-inflammatory cytokines, although the amount of evidence is not yet significant enough. Improved O2 delivery/utilization conferred by hypoxic training interventions might also be effective in preventing and treating cardiovascular diseases, as well as contributing to improve exercise tolerance and health status of patients. For example, in obese subjects, combining exercise with hypoxic exposure enhances the negative energy balance, which further reduces weight and improves cardio-metabolic health. In hypertensive patients, the larger lowering of blood pressure through the endothelial nitric oxide synthase pathway and the associated compensatory vasodilation is taken to reflect the superiority of exercising in hypoxia compared to normoxia. A hypoxic stimulus, in addition to exercise at high vs. moderate intensity, has the potential to further ameliorate various aspects of the vascular function, as observed in healthy populations. This may have clinical implications for the reduction of cardiovascular risks. Key open questions are therefore of interest for patients suffering from chronic vascular or cellular hypoxia (e.g. work-rest or ischemia/reperfusion intermittent pattern; exercise intensity; hypoxic severity and exposure duration; type of hypoxia (normobaric vs. hypobaric); health risks; magnitude and maintenance of the benefits). Outside any potential beneficial effects of exercising in O2-deprived environments, there may also be long-term adverse consequences of chronic intermittent severe hypoxia. Sleep apnea syndrome, for instance, leads to oxidative stress and the production of reactive oxygen species, and ultimately systemic inflammation. Postulated pathophysiological changes associated with intermittent hypoxic exposure include alteration in baroreflex activity, increase in pulmonary arterial pressure and hematocrit, changes in heart structure and function, and an alteration in endothelial-dependent vasodilation in cerebral and muscular arteries. There is a need to explore the combination of exercising in hypoxia and association of hypertension, developmental defects, neuro-pathological and neuro-cognitive deficits, enhanced susceptibility to oxidative injury, and possibly increased myocardial and cerebral infarction in individuals sensitive to hypoxic stress. The aim of this Research Topic is to shed more light on the transcriptional, vascular, hemodynamics, neuro-humoral, and systemic consequences of training at high intensities under various hypoxic conditions.
Clinical practice related to sleep problems and sleep disorders has been expanding rapidly in the last few years, but scientific research is not keeping pace. Sleep apnea, insomnia, and restless legs syndrome are three examples of very common disorders for which we have little biological information. This new book cuts across a variety of medical disciplines such as neurology, pulmonology, pediatrics, internal medicine, psychiatry, psychology, otolaryngology, and nursing, as well as other medical practices with an interest in the management of sleep pathology. This area of research is not limited to very young and old patientsâ€"sleep disorders reach across all ages and ethnicities. Sleep Disorders and Sleep Deprivation presents a structured analysis that explores the following: Improving awareness among the general public and health care professionals. Increasing investment in interdisciplinary somnology and sleep medicine research training and mentoring activities. Validating and developing new and existing technologies for diagnosis and treatment. This book will be of interest to those looking to learn more about the enormous public health burden of sleep disorders and sleep deprivation and the strikingly limited capacity of the health care enterprise to identify and treat the majority of individuals suffering from sleep problems.
Breathing is performed by the rhythmic contraction of respiratory muscles. It ma- tains homeostasis of the organism by taking in the oxygen necessary to live and work and by controlling the level of CO within the organism. At first glance, breathing 2 seems simple; however, it is produced by a complex system in the brain with various afferents and efferents. The control of breathing is of the utmost importance in s- taining life, and although more than 150 years have passed since research on brea- ing control was first begun, many unsolved mysteries still remain. Breathing is like watching the tides at a beach that are created by the vast, complex open sea. The first Oxford Conference on Modeling and Control of Breathing was held 30 years ago in September of 1978 at the University Laboratory of Physiology in Oxford, England. During this first conference, the participants engaged in a hot d- cussion on the problem of whether breathing rhythm was produced by pacemaker cells or a neural network. This was before the discovery of the Bötinger complex in the medulla, and at the time, central chemoreceptive areas were still the focus of research. This conference was an especially unforgettable moment in the dawning of the new age of respiratory research. It has since been held every 3 years in various countries around the globe and is widely appreciated as the best respiratory meeting in the world.
The appearance of photosynthetic organisms about 3 billion years ago increased the partial pressure of oxygen (PO2) in the atmosphere and enabled the evolution of organisms that use glucose and oxygen to produce ATP by oxidative phosphorylation. Hypoxia is commonly defined as the reduced availability of oxygen in the tissues produced by different causes, which include reduction of atmospheric PO2 as in high altitude, and secondary to pathological conditions such as sleep breathing and pulmonary disorders, anemia, and cardiovascular alterations leading to inadequate transport, delivery, and exchange of oxygen between capillaries and cells. Nowadays, it has been shown that hypoxia plays an important role in the genesis of several human pathologies including cardiovascular, renal, myocardial and cerebral diseases in fetal, young and adult life. Several mechanisms have evolved to maintain oxygen homeostasis. Certainly, all cells respond and adapt to hypoxia, but only a few of them can detect hypoxia and initiate a cascade of signals intended to produce a functional systemic response. In mammals, oxygen detection mechanisms have been extensively studied in erythropoietin-producing cells, chromaffin cells, bulbar and cortical neurons, pulmonary neuroepithelial cells, smooth muscle cells of pulmonary arteries, and chemoreceptor cells. While the precise mechanism underpinning oxygen, sensing is not completely known several molecular entities have been proposed as possible oxygen sensors (i.e. Hem proteins, ion channels, NADPH oxidase, mitochondrial cytochrome oxidase). Remarkably, cellular adaptation to hypoxia is mediated by the master oxygen-sensitive transcription factor, hypoxia-inducible factor-1, which can induce up-regulation of different genes to cope the cellular effects related to a decrease in oxygen levels. Short-term responses to hypoxia included mainly chemoreceptor-mediated reflex ventilatory and hemodynamic adaptations to manage the low oxygen concentration while more prolonged exposures to hypoxia can elicit more sustained physiological responses including switch from aerobic to anaerobic metabolism, vascularization, and enhancement of blood O2 carrying capacity. The focus of this research topic is to provide an up-to-date vision on the current knowledge on oxygen sensing mechanism, physiological responses to acute or chronic hypoxia and cellular/tissue/organ adaptations to hypoxic environment.
As 1 review these pages, the last of them written in Summer 1978, some retrospec tive thoughts come to mind which put the whole business into better perspective for me and might aid the prospective reader in choosing how to approach this volume. The most conspicuous thought in my mind at present is the diversity of wholly independent explorations that came upon phase singularities, in one guise or another, during the past decade. My efforts to gather the published literature during the last phases of actually writing a whole book about them were almost equally divided between libraries of Biology, Chemistry, Engineering, Mathematics, Medicine, and Physics. A lot of what 1 call "gathering " was done somewhat in anticipation in the form of cönjecture, query, and prediction based on analogy between developments in different fields. The consequence throughout 1979 was that our long-suffering publisher re peatedly had to replace such material by citation of unexpected flurries of papers giving substantive demonstration. 1 trust that the authors of these many excellent reports, and especially of those I only found too late, will forgive the brevity of allusion I feIt compelled to observe in these substitutions. A residue of loose ends is largely collected in the index under "QUERIES. " It is c1ear to me already that the materials I began to gather several years ago represented only the first flickering of what turns out to be a substantial conflagration.